Ketamine is one of several clinically important drugs whose therapeutic efficacy is due in part to their ability to act upon ion channels prevalent in nearly all biological systems. In studying eukaryotic and prokaryotic organisms in vitro, we show that ketamine short-circuits the growth and spatial expansion of three microorganisms, Stachybotrys chartarum, Staphylococcus epidermidis and Borrelia burgdorferi, at doses efficient at reducing depression-like behaviors in mouse models of clinical depression. Although our findings do not reveal the mechanism(s) by which ketamine mediates its antifungal and antibacterial effects, we hypothesize that a function of L-glutamate signal transduction is associated with the ability of ketamine to limit pathogen expansion. In general, our findings illustrate the functional similarities between fungal, bacterial and human ion channels, and suggest that ketamine or its metabolites not only act in neurons, as previously thought, but also in microbial communities colonizing human body surfaces.

In the olfactory system, the IP3 receptor subtype 3 (IP3R3) is expressed exclusively in a microvillous cell subtype that is the predominant cell expressing neurotrophic factor neuropeptide Y (NPY). We hypothesized that IP3R3-expressing microvillous cells secrete sufficient NPY needed for both the continual maintenance of the neuronal population and for neuroregeneration following injury. We addressed this question by assessing the release of NPY and the regenerative capabilities of wild type, IP3R3(+/-), and IP3R3(-/-) mice. Although the number of mature neurons and the in vivo rate of proliferation were not altered, the proliferative response to the olfactotoxicant satratoxin G and olfactory bulb ablation injury was compromised in the olfactory epithelium of IP3R3(-/-) mice.

The researchers developed a model of Satratoxin G (SG) exposure in monkeys, whose nasal airways resemble those of humans. SG induced acute rhinitis, atrophy of the olfactory epithelium (OE), and apoptosis of OSNs in both groups.

This study demonstrates that neurological system cell damage can occur from satratoxin H exposure to neurological cells at exposure levels that can be found in water-damaged buildings contaminated with fungal growth. The constant activation of inflammatory and apoptotic pathways at low levels of exposure in human brain capillary endothelial cells, astrocytes, and neural progenitor cells may amplify devastation to neurological tissues and lead to neurological system cell damage from indirect events triggered by the presence of trichothecenes.

Satratoxin G (SG), a macrocyclic trichothecene produced by Stachybotrys chartarum, induces apoptosis in cultured neuronal cells as well as nasal olfactory sensory neurons (OSN) in the nose and brain of mice exposed intranasally to this toxin. The purposes of this study were to (1) develop a facile method for production and purification of both SG and its putative biosynthetic precursor, roridin L2 (RL2), from S. chartarum cultures and (2) compare their relative neurotoxicity in vitro and in vivo.

Using an intranasal instillation model in mice, we found that acute Satratoxin G exposure specifically induced apoptosis of olfactory sensory neurons (OSNs) in the olfactory epithelium. These findings suggest that neurotoxicity and inflammation within the nose and brain are potential adverse health effects of exposure to satratoxins and Stachybotrys in the indoor air of water-damaged buildings.

Links on this page are in orange (no underlining).

140

FREE BOOK

Sign up for updates on new information about mold-related illness from Paradigm Change.
You also will receive a free PDF copy of the popular ME/CFS recovery story, Back from the Edge.Click for More Info

.

Search This Website

.

About Paradigm Change

Paradigm Change provides a variety of information on the role of environmental microbial toxins in chronic multsymptom illnesses (including ME/CFS, fibromyalgia, chronic/post Lyme, MCS/EI, POTS, MCAS, Alzheimer’s, autism and other similar conditions).

Information resources offered by Paradigm Change may be accessed at the links below.

Please Note

The information on this site is for educational use only. It is not intended as medical advice.

“Paradigm Change,” “Avoiding Mold,” “Locations Effect,” “Locations Ratings," “Living Clean in a Dirty World," "Mold Avoiders" and "Rabbit Hole" are trademarks belonging to Paradigm Change. Please do not use any of these trademarks as the name of your mold-oriented or health-oriented organization or enterprise without the written permission of Lisa Petrison.

This website may include affiliate links provided by Amazon or other merchants. Paradigm Change may receive a small percentage of sales made subsequent to clicks on those links.